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Pathology Flashcards

1
Q

What are the causes of atheroma?

A
  • high blood pressure (hypertension)
  • diabetes
  • obesity
  • high cholesterol
  • smoking
  • inflammatory diseases such as lupus and rheumatoid arthritis
  • age
  • sex (men and postmenopausal women are at risk)
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2
Q

Describe the mechanism of an atheroma in 5 steps

A
  1. endothelial dysfunction
  2. formation of lipid layer or fatty streak within the intima
  3. migration of leukocytes and smooth muscle cells into the vessel wall
  4. foam cell formation
  5. degradation of extracellular matrix
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3
Q

What are the effects of atheromas?

A
  • In some cases, pieces of the plaque can break away. When that happens, the body responds by producing a blood clot, which can further block artery walls.
  • If atheromas become big enough, they can lead to serious health issues, including heart attack and stroke.
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4
Q

what are the clinical manifestations of atheromas?

A
  • chest pain or angina
  • pain in your leg,arm or anywhere else thay has a blocked artery.
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5
Q

What are the causes of thrombosis?

A
  • disease or injury to the leg veins
  • not being able to move around (immobility)
  • a broken bone (fracture)
  • certain medicines
  • obesity
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6
Q

Name some risk factors of thrombosis

A
  • smoking
  • diabetes
  • high blood pressure
  • high cholesterol
  • lack of activity and obesity
  • poor diet
  • family history of arterial thrombosis
  • lack of movement, such as after surgery or a long trip.
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7
Q

What are the clinical manifestations of thrombosis?

A
  • pain in one leg (usually calf or inner thigh)
  • swelling in the leg or arm
  • chest pain
  • numbness or weakness on one side of the body
  • sudden change in your mental state
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8
Q

What is Virchow’s triad?

A

The three factors which are critically important in the development of venous thrombosis:

  1. venous stasis
  2. activation of blood coagulation
  3. vein damage
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9
Q

Name 4 possible complications of pneumonia

A
  1. Involvement of pleural surface- pleurisy (can cause fibrous adhesions), pleural effusion
  2. Tissue necrosis and abscess formation-fistula to the pleura- empyema or pneumothorax
  3. bacteraemia-inflammation at other sites, abscesses in other organs
  4. sepsis
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10
Q

What is the name given to colon cancer?

A

Adenocarcinoma

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11
Q

At some sites most cancers are of one histological subtype. Which is the most common?

A

adenocarcinoma

other forms of tumour are uncommon

  • lymphoma
  • neuroendocrine tumours
  • GIST
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12
Q

On resection specimens or with other biopsy samples (eg from the liver) histology contributes to tumour staging. what does this impact on?

A

treatment decisions and prognosis

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13
Q

what are the objectives of cancer staging?

A
  • to document the extent of the disease
  • this has an impact on treatment decisions
  • not all disease can be detected:
    • radiologically or clinically (either before or after surgery)
    • the full extent of disease at the primary site, extent of invasion and the presence of metastatic disease may only be fully appreciated by microscopy.
    • fibrosis can mimic cancer-histology discriminates
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14
Q

Why are histological landmarks key in pathology?

A

For accurate pathological staging of cancer

  • histological diagnosis and staging are key discussion points at MDTs
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15
Q

What are the 4 T stages in the TNM classification?

A
  • T1-invasion of sub-mucosa
  • T2- invasion of muscularis propria
  • T3- invasion to subserosa and non-peritonealised pericolic and pararectal tissues
  • T4- invasion of adjacent organs or perforation of visceral peritoneum.
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16
Q

What are the 3 N stages of the TNM classification?

A
  • N0- no regional lymph node metastasis
  • N1- 1-3 regional nodes contain metastatic tumour
  • N2- 4 or more nodes contain metastatic tumour
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17
Q

What are the 2 M stages of the TNM classificartion?

A
  • M0- no distant metastasis
  • M1-distant metastasis
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18
Q

The pneumonic VINDICATE gives the causes of disease, what are they?

A
  • Vascular
  • Infectious/Inflammatory
  • Neoplastic
  • Drugs/Toxins
  • Intervention/iatrogenic
  • Congenital/developmental
  • Autoimmune
  • Trauma
  • Endocrine/metabolic
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19
Q

What does iatrogenic mean?

A
  • disease related to medical intervention
  • recognised complications of treatments and procedures
  • sometimes risks are unavoidable
  • need to be aware of these- informed consent
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20
Q

Describe some key facts about endocrine disorder and give an example

A
  • very common
  • diabetes mellitus
  • pituitary, thyroid, parathyroid and adrenal glands
  • inborn errors of metabolism
  • inflammatory processes (often auto-immune)
  • tumours- benign and malignant
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21
Q

Provide some key facts on metabolic causes of disease and give an example

A
  • many disease processes
  • obesity
  • overlap with endocrine disorders
  • inborn errors of metabolism
  • haemachromatosis (Fe)
  • Wilson’s disease (Cu)
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22
Q

What is tissue homeostasis a balance between?

A

Cell division and cell loss

  • regulation of induction of sensecence
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23
Q

What are the two types of stress to which our bodies are subject?

A

Environmental and endogenous

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24
Q

What can happen if changes due to stress are severe?

A

There may be cellular injury or death with associated damage to tissue and organ structure and function.

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25
Q

There are __________ mechanisms that can enable cells to cope with stimuli that are potentially injurous

A

adaptive

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26
Q

What are the 5 causes of cellular/tissue injury?

A
  1. physical- mechanical, thermal, electric, barotrauma
  2. chemical- drugs, metabolic, hypoxia, nutrition
  3. infectious- cytolysis, toxins, immune response
  4. immunological- may contribute to other categories
  5. Genetic- may contribute to other categories
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27
Q

What are the 2 phases of cellular injury?

A

Reversible and irreversible

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28
Q

How are the phases of cellular injury recognised?

A

By morphological features and biochemical features.

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29
Q

What does severe damage/injury of a cell lead to?

A

cell death

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30
Q

Describe how adaptive responses play a role in reversible/irreversible cell injury

A
  • adaptive response can protect the cells and could be a prompt return to normality
  • at the reversible stage the damaging agent may be transient
  • there is a threshold beyond which a cell cannot recover.
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31
Q

What are the intracellular systems vulnerable to cellular injury?

A
  • cell membrane integrity
  • aerobic respiration
  • protein synthesis
    • enzymes
    • structural proteins
  • genomic integrity
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32
Q

Name 5 types of revesible cell damage

A
  1. membrane pump fails
  2. cell swelling
  3. accumulation of lipids
  4. reduced aerobic respiration
  5. increased anaerobic respiration
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33
Q

Give a definition of irreversible damage to cells

A

Precise definition is difficult

characterised by

  • Severe damage to cell membranes
  • severe damage to mitochondria
  • leakage of enzymes
  • nuclear changes
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34
Q

What are two characteristics of irreversible cell damage?

A

ATP depletion

Cell Membrane Damage

  • progressive loss of phospholipids
  • increased degradation
  • reduced synthesis
  • lipid breakdown products
  • Reactive oxygen species
  • cytoskeletal abnormalities
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35
Q

What are the two types of cell death?

A
  • necrosis
  • apoptosis
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36
Q

Describe apoptosis

A
  • physiological or
  • pathological
  • affects scattered cells
    • cells shrink
    • apoptotic bodies form
    • no inflammation
  • energy dependent
    • stereotypes sequence of events
    • biochemical regulation
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37
Q

Decribe necrosis

A
  • always pathological
  • affects sheets of cells
    • cells swell
    • dissolution of organelles
    • inflammation
  • not energy dependent
  • descriptive terms
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38
Q

What are the two terms used if there is injury and damage and then attempted repair which is completed?

A

Regeneration

Restitution

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39
Q

What happens if there is injury and damage and then attempted repair which is incomplete? (2 terms)

A

Repair

Scarring

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40
Q

What 3 things is the outcome of cell injury affected by?

A
  1. The type of cell affected
  2. The damaging agent
  3. other host factors
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41
Q

How does the type of cell affected influence the outcome of cell injury?

A
  • adaptive capability of the affected cell
  • pre-existing disease
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42
Q

How does the damaging agent affect the outcome of cell injury?

A
  • duration/severity of exposure
  • damage that affects structures required for healing e.g. blood vessels with radiation
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43
Q

State the three classifications of cell type

A
  1. Labile
  2. Stable
  3. Permanent
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44
Q

Give 2 examples of where labile cells are found

A
  • GI tract
  • bone marrow
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45
Q

Give 2 examples of stable cells

A
  • hepatocytes
  • endothelium
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46
Q

Give 2 examples of permanent cells

A
  • neurones
  • skeletal muscle
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47
Q

What are labile cells?

A

Ones which are in the active cell cycle all of the time.

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48
Q

What are stable cells?

A

Ones which under normal circumstances do not show that they are in the cell cycle but if required can replace lost cells.

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49
Q

What are permanent cells?

A

They have no capacity in post-natal life for further mitotic divisions, return to normal is not possible.

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50
Q

Which cell populations are capable of complete repair (restitution)?

A

Labile and stable cells

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51
Q

How must death of permanent cell populations be repaired?

A

With scar tissue formation

  • Tissue architecture must be preserved

Examples:

  • lobar pneumonia
  • hepatitis A
  • mild burns
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52
Q

How does repair with scarring proceed? (4 points)

A
  • follows injury with damage to tissue architecture
  • requires formulation of granulation tissue
  • proceeds through organisation to fibrosis (scarring)
  • fibroous scar contracts- by up to 80%- reduces apparent damaged area
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53
Q

For repair with scarring what are the first and second intentions?

A

First intention- surgical scar

  • closely apposed edges
  • minimal granulation tissue
  • minimal fibrosis
  • (langer’s lines)

Second intention- ulcerated surface

  • edges widely separated
  • prominent granulation tissue
  • prominent fibrosis
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54
Q

What are the local factors which influence wound healing?

A
  • type of cell/tissue
  • type of injury
  • foreign material
  • infection
  • blood supply
  • nerve supply
  • local disease e.g. neoplasia
  • stability
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55
Q

What are the systemic factors which influence wound healing?

A
  • age
  • general health
    • nutrition
      • general diet
      • vitamin C
    • specific diseases
      • diabetes mellitus
      • immunodeficiency
    • drugs
      • steroids
      • cytotoxic drugs
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56
Q

What are the local factors which influence the healing of fractures?

A
  • type of injury
    • comminution, compound
  • foreign material
    • exogenous, interposed soft tissues
  • infection
  • blood supply
  • nerve supply
  • local disease
    • neoplasia, osteoperosis
  • stability/alignment
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57
Q

Why are stability/alignment important local factors which influence the healing of fractures?

A
  • stability is important to ensure the bone ends are nipped together and no osteoarthritis
  • alignment is important so the forces transmitted through the bones into the joints are not such that the joints will later become damaged.
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58
Q

What are the 2 types of excessive scar formation?

A
  • hypertrophic scar
  • keloid
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59
Q

What kind of mechanisms do we have that can enable cells to cope with stimuli that are potentially injurous?

A

adaptive mechanisms

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60
Q

What type of adaptations occur as a result of increased demand?

A
  • hypertrophy
  • hyperplasia
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61
Q

What type of adaptation occurs as a result of decreased demand?

A

Atrophy

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62
Q

What type of adaptations occur as a result of altered stimulus?

A
  • metaplasia
  • modified metabolism
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63
Q

Define hypertrophy

A

An increase in cell size

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64
Q

Provide 4 key points about hypertrophy including the types of muscle where it occurs

A
  • May occur in isolation in non-dividing cells
  • otherwise can accompany hyperplasia
  • often a response to mechanical stress
  • muscle:
    • skeletal
    • cardiac
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65
Q

Hypertrophy becomes pathologic in the heart when the function of the heart is compromised. How can this present and why?

A
  • may present as heart failure-inability of the heart to pump as normal
  • the increased bulk of muscle and high pressures generated in the subendocardial regions may cause ischaemia with further damage to and loss of myocytes
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66
Q

Define atrophy

A

Reduction of cell size and number in an organ that was of normal size.

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67
Q

Provide 5 possible causes of atrophy

A
  • Ageing
  • Lack of use/stimulation
    • mechanical
    • functional
  • loss of blood supply
  • malnutrition
  • mechanical pressure
    • e.g. hydronephrosis, hydrocephalus
    • can be seen in normal tissue adjacent to tumours
    • pituitary adenoma
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68
Q

Describe cerebral atrophy

A
  • decreased brain size with ageing
  • impaired blood supply and ischaemic damage may contribute
    • may be associated with atherosclerosis
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69
Q

What are the cellular mechanisms of atrophy?

A
  • reduced cellular components
  • protein degradation
  • “digested” in lysosomes and degraded in many cases by ubiquitin proteasome pathway
  • some hormones promote degradation and atrophy- glucocorticoids and thyroid hormone
  • some oppose atrophy and promote growth-insulin
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70
Q

How does atrophy contribute to homeostasis?

A

A balance of growth and atrophy retains homeostasis.

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71
Q

Define hyperplasia

A

An increase in cell number in response to a stimulus.

  • results in increased size/volume of an organ or tissue
  • regresses on withdrawal of the stimulus.
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72
Q

Is hyperplasia physiological or pathological?

A

Both as it can be compensatory/regenerative

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73
Q

Which 3 organs are hormonally sensitive for hyperplasia?

A
  • endometrium
  • breast
  • thyroid
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74
Q

Describe compensatory hyperplasia

A
  • occurs after loss of tissue
  • not common in many tissues
  • liver is the most obvious example
  • bone marrow
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75
Q

Name one way pathological hyperplasia can be induced and whether it can regress?

A

hormonally

yes with withdrawal of stimulus

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76
Q

Give 2 examples of pathological hyperplasia

A
  • hormonally induced excess oestrogen leads to endometrial hyperplasia and abnormal menstrual bleeding. often post menopausal
  • hormonally induced prostatic hyperplasia. In response to androgens
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77
Q

What is enlargement of the gingival tissues an example of?

A
  • Hyperplastic responses within epithelium and underlying connective tissue
  • various causes including certain drugs
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78
Q

Define hypoplasia

A

Reduced size of an organ thaat never fully developed to a normal size.

  • a developmental defect
  • e.g. pulmonary hypoplasia
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79
Q

What are metabolic adaptations and metaplasia?

A

Acquired alterations in gene expression

  • associated with altered metabolic capability within the cells eg in cancer cells in response to cytotoxic drugs
  • or features of altered differentiation
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80
Q

Define metaplasia

A
  • An acquired form of altered differentiation
  • probably reflects altered differentiation pathways from multipotent stem cells
  • one fully mature cell type to another fully mature cell type
  • can be part of an adaptive response to stress
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81
Q

Give some examples of where metaplasia can occur

A
  • cervix
  • bronchus
  • salivary ducts
  • Barrett’s oesophagus- if there is reflux of gastric contents into the oesophagus the squamous endothelium is damaged. Over time there is loss, ulceration and inflammation. When the area is repaired they are a different type- more closely alligned, adaptive resposne.
  • can also affect mesenchymal tissues
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82
Q

Is metaplasia a neoplastic disorder

A

No

  • environmental changes leading to metaplasia may if persistent lead to further changes that can manifest as dysplasia and progress to malignancy (cancer) e.g. barretts oesophagus
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83
Q

Name the 3 inhibitors of apoptosis

A
  • growth factors
  • cell matrix components
  • viral proteins
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84
Q

What are the inducers of apoptosis?

A
  • withdrawal of growth factors
  • loss of matrix attachment
  • viruses
  • free radicals
  • ionising radiation
  • DNA damage
  • Fas ligand/CD95 interaction
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85
Q

What are the molecular mediators and regulators in the extrinsic pathway for apoptosis?

A

death receptors e.g. CD95/Fas ligand

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86
Q

What are the molecular mediators and regulators of the intrinsic pathway of apoptosis?

A
  • increased mitochondrial permeability
  • Bcl-2 family
  • cytochrome c/Apaf-1
  • can induce OR inhibit
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87
Q

Name 2 molecular mediators and regulators of apoptosis

A
  • p53
  • caspases-cascade
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88
Q

Give 3 situations where there is increased apoptosis

A
  • AIDS
  • neurodegenerative disorders
  • reperfusion injury
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89
Q

Give 2 examples of where there would be decreased apoptosis

A
  • neoplasia
  • auto-immune disease
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90
Q

What is inflammation?

A
  • A local physiological response to tissue injury
  • A complex reaction in vascularised connective tissue
  • reaction of blood vessels which leads to accumulation of fluid and leukocytes in extravascular tissues
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91
Q

What is the purpose of inflammation?

A
  • serves to destroy, dilute or wall off the injurious agent
  • primarily a protective response intertwined with the process of repair.
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92
Q

What would happen without inflammation?

A
  • wounds and injured organs would never heal
  • infections would go unchecked
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93
Q

In what ways could inflammation and repair be potentially harmful?

A
  • life-threatening hypersensitivity reactions
  • chronic inflammatory diseases eg rheumatoid arthritis and crohns disease
  • repair by fibrosis may lead to problems such as disfiguring scars
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94
Q

Name the 2 types of inflammation

A
  • acute
  • chronic
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95
Q

What are the 5 principle causes of acute inflammation?

A
  1. Infections e.g. viruses, bacteria, fungi
  2. hypersensitivity reactions- inappropriate or excessive immune response which damages the tissues incl reactions to parasites
  3. physical agents e.g. physical trauma, UV light, thermal injury (burns or frostbite)
  4. Irritant and corosive chemicals e.g. acids, alkalis, infecting agents releasing chemical irritants
  5. foreign bodies e.g. splinters, dirt, sutures
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96
Q

Name the 5 physical characteristics of inflammation

A
  1. Redness (rubor)
  2. heat (calor)
  3. swelling (tumor)
  4. pain (dolor)
  5. loss of function
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97
Q

Why do acutely inflamed tissues appear red?

A

due to dilation of small blood vessels within the damaged area.

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98
Q

Why is there production of heat during inflammation?

A

Increase in temperature of the tissue due to increased blood flow through the region (hyperaemia)

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99
Q

Why is there swelling during acute inflammation?

A

Results from accumulation of fluid in the extravascular space (fluid exudate)

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100
Q

Why is pain a characteristic of inflammation?

A

Due to stretching and distortion of tissues caused by increased fluid. Various chemical mediators, including bradykinin are known to produce pain.

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101
Q

Why is loss of function a characteristic of inflammation?

A

Movement of the inflamed area is consciously and reflexly inhibited by pain. severe swelling may immobilise tissues.

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102
Q

The initilal rapid reactionof tissue to injury involves several processes split into 2 phases. Name these phases

A
  1. vascular phase
  2. exudative and cellular phase
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103
Q

What are the two processes involved in the vascular phase?

A
  • vasodilation
  • increased permeability of blood vessels
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104
Q

What is the the result of vasodilation?

A

Increased blood flow and thus heat and redness

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105
Q

Describe the steps involved in the increased permeability of blood vessels in the vascular phase.

A
  • small blood vessels are lined by a single layer of endothelial cells
  • the walls of small vessels act as a microfilter
  • oxygen, CO2 and some nutrients transfer across the wall by diffusion
  • In AI permeability increases due to the formation of endothelial gaps in the venules
  • endothelial cells contain contractile proteins, when stimulated by chemical mediators they pull open transient pores
  • chemical mediators include histamine and bradykinin
  • endothelial cell are NOT damaged in this process
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106
Q

Where is leakage of fluid confined to when the increased permeability of blood vessels occurs?

A

POST CAPILLARY VENULES

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107
Q

What happens during the exudative and cellular phase of acute inflammation?

A
  • fluid and cells escape from permeable venules
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108
Q

What is the name given to the net increase in extravascular fluid as a result of the exudative and cellular phase?

A

Oedema

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109
Q

Describe the fluid exudate

A
  • proteins incl immunoglobulins, important in destruction of invading organisms
  • fibrinogen –> fibrin on contact with the extracellular matrix, so AI organ surfaces commonly covered by fibrin
  • exudate is continually removed by lymphatics and replaced
  • antigens are carried to regional lymph nodes for recognition by lymphocytes
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110
Q

How is the extent of oedema in tissues limited in AI?

A

The lymphatic channels become dilated as they drain away the oedema fluid of the inflammatory exudate

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111
Q

What is the diagnostic feature of acute inflammation?

A

Accumulation of neutrophils in the extracellular space

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112
Q

What is another name given to neutrophils?

A

polymorphonuclear leucocytes

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113
Q

State the functions of neutrophils

A
  • kill microorganisms
  • ingest offending agents
  • degrade necrotic tissue
  • produce chemical mediators
  • produce toxic oxygen radicals
  • produce tissue damaging enzymes
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114
Q

How does a neutrophil reach the site of an inflammatory stimulus?

A

By a combination of different processes involving adhesion of circulating leucocytes to endothelial cells and subsequent migration through the endothelium.

  1. margination
  2. adhesion
  3. transendothelial migration
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115
Q

Describe margination

A

Normally blood cells flow in the centre of the lumen (axial flow)- the area adjacent to the blood vessel wall carries only plasma.

Loss of intravascular fluid and increased plasma viscosity slows flow allowing neutrophils to flow in the plasmatic zone- this is MARGINATION

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116
Q

Where is the only place margination occurs?

A

Venules

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117
Q

How does increased neutrophil adhesion occur?

A

It results from the interaction between adhesion molecules on the neutrophils surface and the endothelial surface.

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118
Q

What does loose, rolling adhesion involve?

A

Selectins on the surface of activated endothelial cells and their receptors on the leucocyte.

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119
Q

How does firm adhesion occur?

A

Between activated integrins on the leucocyte and members of the immunoglobulin supergene family including ICAM-1 (intracellular adhesion molecule 1) and VCAM-1 (vascular cell adhesion) on the endothelial cell.

120
Q

Describe transendothelial migration?

A

Once firm adhesion to the endothelium has been achieved, neutrophils insert pseudopodia into the junctions between endothelial cells.

They then cross through the basement membrane into the extravascular space.

121
Q

How is transmigration mediated?

A

By ICAM-1, integrins and platelet/endothelial cell adhesion molecule-1 (PECAM-1 or CD31)

122
Q

How do neutrophils find the site of the inflammatory stimulus?

A

By a process called chemotaxis

123
Q

Define the process chemotaxis

A

locomotion orientated along a chemical gradient.

124
Q

Name 4 compounds chemotatic for neutrophils

A
  • bacterial products
  • complement components
  • cytokines
  • products produced by neutrophils themselves
125
Q

Once at the site of inflammation neutrophils are involved in removing injurious agent eg bacteria by a process called ______________.

A

Phagocytosis

126
Q

What is phagocytosis?

A

The complex process by which phagocytes such as neutrophils and macrophages engulf and ingest micoorganisms or other cells and forgein particles.

127
Q

State the 3 steps of phagocytosis

A
  1. recognition and attachment
  2. engulfment
  3. killing and degradation
128
Q

How is efficiencyof phagocytosis generally enhanced?

A

When particles are opsonized

129
Q

What is opsonization?

A

The process of coating a particle to target it for phagocytosis.

  • most micro-organisms are not recognised until coated in opsonins
130
Q

What do opsonins do?

A

Bind to specific receptors on leucocytes and greatly enhance phagocytosis

e.g. Fc fragment on IgG

131
Q

How is the process of active phagocytosis initiated?

A

By attachment of a particle to a phagocyte receptor

132
Q

What does engulfment involve?

A

Cytoplasmic extensions to flow around the particle resulting in complete ‘engulfment’ of the particle within a phagosome made by the cell membrane.

133
Q

What happens after engulfment?

A

The phagosome membrane then fuses with lysosomal membrane, resulting in discharge of the lysosome content into the phagolysosome.

134
Q

What are the two types of mechanism for killing of infectious agents?

A
  1. Oxygen-dependent
  2. Oxygen-independent
135
Q

How does oxygen-dependent killing occur?

A

Phagocytosis results in products of oxygen reduction which cause intracellular killing of micro-organisms.

136
Q

How does oxygen independent killing occur?

A

via the action of substances in leukocyte granules

eg

  • lysozyme which attacks bacterial coat
  • defensins that are cytotoxic to microbes
  • acidic pH inside phagolytic vacuoles
137
Q

What happens to the microorganisms inside of the phagolysosome after killing?

A

Acid hydrolase from lysosomes degrades them

138
Q

During activation and phagocytosis what happens to the leucocyte products?

A

They are released into the EXTRACELLULAR SPACE as well as into phagolysosome.

139
Q

What are the effects of lysosomal product release?

A

These products may cause endothelial and tissue damage

  1. activates coagulation factor XII
  2. attracts other leukocytes into the area
  3. damage local tissues
  4. increases vascular permeability
  5. pyrogens producing systemic fever
140
Q

What happens to neutrophils after apoptosis?

A

They undergo apoptosis which is pre-programmed cell death.

141
Q

What is the name of chemicals which drive the process of inflamation?

A

ENDOGENOUS chemical mediators

142
Q

Where can endogenous chemical mediators be found?

A

May be made in and released by inflammatory cels or circulate in plasma.

143
Q

What are the five mediated processes of acute inflammation?

A
  1. vasodilation
  2. emigration of neutrophils
  3. chemotaxis
  4. increased vascular permeability
  5. itching and pain
144
Q

Why are chemical mediators of acute inflammation important?

A

For therapeutic reasons eg antihistamines

145
Q

What are the chemical mediators of inflammation released from cells?

A
  • Histamine
  • serotonin
  • platelet-activating factor
  • metabolites of Arachidonic Acid (leukotrienes, prostaglandins)
146
Q

Describe the release of histamine as a chemical mediator of AI

A
  • mast cells in connective tissue most important source
  • also in circulating basophils and platelets
  • arteriolar dilation and increase in venule permeability
  • release of histamine is stimulated by various factors including C3a, C5a
147
Q

Where is serotonin present in high concentration?

A

In platelets

148
Q

What does seratonin do?

A

Causes dilation of arterioles and increased venule permeability

149
Q

Describe platelet activating factor (PAF) as a chemical mediator

A
  • made in leukocytes and endothelial cells in response to inflammatory stimuli
  • increases venule endothelial permeability and leukocyte/endothelial adhesion.
150
Q

How is arachidonic acid metabolised? (2 main pathways)

A
  1. cyclooxygenase (COX) pathway
  2. lipoxygenase pathway
  • membrane lipids are metabolised to produce chemical mediators during cell activation of the inflammatory response.
151
Q

Cyclocygenase (COX) pathway leads to the production of prostaglandins, what do these do?

A

Promote vasodilation and increase vascular permeability

152
Q

Lipoxygenase pathway leads to production of leukotrienes, what is their purpose?

A

Possess vasoactive and chemotactic properties.

153
Q

Why are the COX and lipoxygenase pathways important?

A

Many anti-inflammatory drugs used in clinical practice target them,

154
Q

Plasma contains 4 enzymatic cascade systems which mediate various aspects of inflammation in addition to other functions. Name them.

A
  1. complement system
  2. coagulation system
  3. kinin system
  4. fibrinolytic system
155
Q

What does acute inflammation look like under the microscope?

A

The diagnostic feature of acute inflammation is neutrophil accumulation in the extracellular space.

156
Q

Name and describe the 6 macroscopic appearances of acute inflammation

A
  • necrotising- septic necrosis
  • serous- thin protein rich fluid exodate
  • catarrhal-mucus hypersecretion
  • fibrinous- exudate contains plentiful fibrin
  • suppurative- production of pus
  • membranous- epithelium coated by fibrin
157
Q

At a histological level what does pus contain?

A
  • neutrophils
  • micro-organisms
  • cellular debris
158
Q

What is the definition of an ulcer?

A

A local defect, or excavation, of the surface of an organ or tissue that is produced by the sloughing (removal) of inflammatory nectoric tissue

159
Q

Where are ulcers most frequently seen?

A
  • mucosa of the mouth
  • GI tract
  • GU tract
  • low limbs (chronic ulcers) in those with circulatory disturbance
160
Q

What are the 6 beneficial effects of acute inflammation?

A
  1. dilution of toxins-can be carried away by lymphatics
  2. entry of antibodies- due to increased vascular permeability
  3. stimulation of the immune response- fluid exudate containing antigens reaches local lymph nodes
  4. fibrin formation- impedes movement of micro-organisms
  5. delivery of nutrients and oxygen-aided by blood flow
  6. transport of drugs- eg antibiotics
161
Q

What are the 3 harmful effects of acute inflammation?

A
  • Digestion and damage of normal tissues.
  • swelling- eg laryngeal oedema, brain swelling
  • inappropriate inflammatory response- eg type I hypersensitivity
162
Q

What are 5 systemic effects of acute inflammation?

A
  1. fever
  2. constitutional symptoms
  3. weight loss
  4. reactive hyperplasia of the reticuloendothelial system
  5. haematological changes
163
Q

How and why does fever occur in AI?

A
  • one of the most prominent systemic manifestations, particularly when inflammation is associated with infection
  • due to effects of IL-1 and TNF acting on the hypothalamus to reset thermoregulatory mechanisms to a higher temperature
  • elevation in temp of even a few degrees may improve the efficacy of leukocyte killing and probably impairs the replication of many offending micro-organisms
  • blood is redirected from the skin to deep vascular beds to minimize heat loss through the skin.
  • increased pulse and BP
  • decreased sweating
  • production of acute phase proteins by the liver including C-reactive protein (CRP), serum amyloid A protein, serum amyloid P protein and coagulation/complement proteins.
  • increased production of glucocorticoids activating a stress response.
  • rigors (shivering)
  • loss of apetite
  • drowsiness
  • malaise- general feeling of unwell
164
Q

Name some constitutional symptoms of AI

A
  • malaise
  • loss of apetitie
  • nausea
165
Q

Describe reactive hyperplasia of the reticuloendothelial system as a systemic effect of acute inflammation

A

Nodal enlargement is caused by hyperplasia of lymphoid follicles and hyperplasia of the phagocytic cells lining the sinuses.

166
Q

What are the haematological changes caused by Acute inflammation?

A
  • increased erythrocyte sedimentation rate (SER)
  • anaemia eg blood loss
  • leucocytosis eg lymphocytosis, neutrophilia, eosinophilia (an increased no. of WBCs in the circulation)
167
Q

What is the usual cause of leucocytosis?

A

Usually due to accelerated release of cells from the bone marrow reserve pool (IL-1 and TNF).

168
Q

What do most bacterial infections produce?

A

A neutrophilia

169
Q

What do most viral infections produce?

A

lymphocytosis

170
Q

What is normally produced in allergic disorders and parasitic infection?

A

eosinophilia

171
Q

What are the possible sequelae of acute inflammation?

A
  • resolution
  • suppuration/abscess formation
  • chronic inflammation
  • healing by fibrosis and scar formation
172
Q

define resolution

A

Resolution is where the tissue returns completely to normal after acute inflammation. It can only occur under certain circumstances

173
Q

What are 5 factors which favour resolution?

A
  • minimal cell death and tissue damage
  • tissue architecture must be preserved
  • occurence in an organ or tissue with regenerative capacity eg liver
  • rapid detruction of the causal agent
  • rapid removal of fluid and debris by good local vascular drainage.
174
Q

In which populations of cells does resolution occur?

A

labile and stable cell populations

175
Q

How must death of permanent cell populations be repaired?

A

With scar tissue formation

176
Q

What are the three classifications of cell type?

A

Labile

Stable

Permanent

177
Q

What are labile cells? give 2 examples of where they are found.

A

Ones which multiply continuously throughout life

e.g. GI tract, bone marrow

178
Q

What are stable cells? Give 2 examples of where they are found.

A

Stable cells are ones that only multiply when they receive the stimulus to do so

e.g. hepatocytes, endothelium

179
Q

What are permanent cells? Give 2 examples of where they are found

A

Permanent cells are ones which cannot multiply e.g. neurones and skeletal muscle

180
Q

What is suppuration?

A

Formation of pus- neutrophils, bacteria, cellular debris

181
Q

The causative stimulus of suppuration/abscess formation is almost always what?

A

An infective agent eg pyogenic bacteria such as staphylococci

182
Q

Descrive an abscess

A

An abscess has a central collection of pus with an adjacent zone of preserved neutrophils surrounded by a membrane of sprouting capillaries, vascular dilation and occasional fibroblasts.

183
Q

what happens when an abscess is drained?

A

On draining an abscess, cavity collapses and is obliterated by organisation and fibrosis.

184
Q

Where may deep seated asbscesses drain?

A

Along a sinus tract or fistula.

185
Q

What are the 2 ways in which chronic inflammation may arise?

A
  1. chronic inflammation developing from acute inflammation
  2. primary chronic inflammation
186
Q

When might inflammation shift from accute to chronic?

A

If the agent causing the acute inflammation is not removed.

In addition to organisation of the tissue the character of the cellular exudate changes.

187
Q

State 3 factors which favour the progression from acute to chronic inflammation

A
  1. indigestible substances such as glass and suture material
  2. deep seated suppurative inflammation in which drainage is delayed or inadequate will result in a thick abscess wall composed of fibrous/granulation tissue.
  3. recurrent episodes of acute inflammation and healing may eventually result in the clinicopathological entity of chronic inflammation.
188
Q

How can chronic inflammation be defined? What are the predominant cells?

A

May be defined as an inflammatory process in which lymphocytes, plasma cells and macrophages predominate.

Usually accompanied by the formation of granulation tissue resulting in fibrosis.

A few eosinophils may be present but neutrophil polymorphs are scarce.

189
Q

Besides different immune cells being present, what else is different about chronic inflammation in compared to acute?

A

less oedema

fewer alterations in blood flow.

190
Q

Provide 6 examples of primary chronic inflammation

A
  1. resistance of infective agent to phagocytosis and intracellular killing e.g. TB, leprosy, viral infections
  2. foreign body reactions to endogenous materials eg gout (may be acute or chronic)
  3. foreign body reactions to exogenous materials eg asbestos
  4. some autoimmune diseases eg rheumatoid arthritis
  5. specific diseases of unknown aetiology eg ulceritive colitis
  6. primary granulomatous diseases eg sarcoidosis
191
Q

What are the macroscopic appearances of chronic inflammation?

A
  • chronic ulcer
  • chronic abscess cavity eg osteomyelitis
  • thickening of the wall of a hollow organ by fibrous tissue eg inestine
  • granulomatous inflammation eg tuberculosis (caseous necrosis)
192
Q

What can be the most prominent feature of the chronic inflammation reaction?

A

fibrosis

when most of the chronic inflammatory cell infiltrate has subsided, fibrosis may lead to distortion and stricture formation eg crohn’s disease

193
Q

How do macrophages play a key role in chronic inflammation?

A
  • monocytes leave the circulation and undergo chemotaxis similar to neutrophils. monocytes in the tissues are called macrophages.
  • relatively large cells which possess considerable phagocytic capabilities.
  • capable of ingesting a wide range of materials
  • can harbour viable organisms resistant to lysosomal enzymes eg mycobacterium TB, Mycobacterium leprae
  • produce a range of important cytokines
194
Q

What is granulomatous inflammation?

A

A specific pattern of chronic inflammaton

195
Q

What is a granuloma?

A

An aggregate of epitheliod histiocytes

196
Q

What is a histiocyte?

A

A macrophage present in connective tissue.

197
Q

Why might a granuloma form?

A

Formation may be immune-mediated or may be in response to foreign matter difficult to clear.

198
Q

Name the 3 causes of granulomatous inflammation

A
  • Specific infections (mycobacteria eg TB)
  • foreign bodies
    • endogenous eg keratin
    • exogenous eg suture material, asbestos
  • unknown eg crohn’s
199
Q

How does healing by fibrosis and scar formation occur?

A

Tissue destruction includes loss of parenchymal cells and associated stromal framework.

whilst some tissue has regenerative capacity to replace parenchymal cells, others do not thus non-regenerated parenchymal cells are replaced by connective tissue (granulation tissue) which in time produces fibrosis and scarring.

200
Q

What are the 4 steps involved in the repair by connective tissue fibrosis?

A
  1. angiogenesis- formation of new blood vessels
  2. migration, activation and proliferation of fibroblasts/myofibroblasts
  3. deposition of collagen
  4. remodelling and maturation of fibrous tissue to form a scar
201
Q

What do angiogenesis and fibroblast proliferation lead to?

A

Formation of granulation tissue

202
Q

What is granulation tissue composed of?

A
  • Fibroblasts
  • endothelial cells
  • macrophages
  • collagen
  • extracellular matrix components
203
Q

What is organisation of tissues?

A

Their replacement by granulation tissue.

204
Q

What are 3 factors which favour organisation?

A
  • Large amounts of fibrin formed
  • substantial necrosis
  • exudate and debris cannot be removed or discharged
205
Q

Although functionally _________, scarring provides a _________ patch allowing the residual parenchyma to more or less continue functioning.

A

Imperfect

Permanent

206
Q

Give 2 examples where a scar might be so large or sited it causes dysfunction

A
  1. inflammatory bowel disease- fibrous tissue may cause a colonic structure
  2. healed myocardial infarct- fibrous tissue replaces contractile muscle
207
Q

What are the two types of repair with scarring?

A
  • First/primary intention
  • secondary intention
208
Q

What conditions lead to first intention scarring?

A
  • Surgical incision
  • closely apposed edges
  • minimal granulation tissue
  • minimal fibrosis
209
Q

What conditions lead to second intention scarring?

A
  • Ulcerated surface
  • edges widely separated
  • prominent granulation tissue
  • prominent fibrosis
210
Q

What are 4 local factors that influence wound healing?

A
  • infection- single most important cause of delay in healing
  • mechanical factors- ie early motion of wounds delays healing
  • foreign bodies- ie sutures or glass
  • size, location and type of wound- wounds heal better in richly vascularised areas
211
Q

State 4 systemic elements which influence wound healing

A
  • nutrition- wound healing profoundly influenced by ability to synthesise protein and collagen
  • metabolic status- diabetes is associated with delayed healing
  • circulatory status- an adequate vascular supply is essential for normal cellular function (hypoxia, reduced local nutrition)
  • hormones- glucoroticoids are anti-inflammatory but impair collagen synthesis
212
Q

What are 3 possible pathological aspects of wound repair?

A
  1. deficient scar formation- wound dehiscence/ulceration
  2. excessive formation of repair components- keloid scar
  3. formation of contractures- exagerrated contraction results in deformity of the wound and surrounding tissues
213
Q

What is anthracotic pigmentation a result of?

A

Inhalation of pollutants

214
Q

What is cellular senescence?

A
  • The cellular response/process where cells withdraw from the cell cycle.
  • cells lose capacity to proliferate in response to mitogenic stimuli
  • altered morphological feature
  • altered expression of proteins
215
Q

What is replicative senescence?

A

After a fixed number of divisions all cells enter a non-dividing state- senescence.

216
Q

What does telemorase do?

A

telemorase in certain cell types (such as stem and germ) allows you to maintain telomere length. This is lost in somatic cells though so they enter replicative sensecence.

217
Q

Which diseases are common in the elderly?

A
  • cardiovascular disease
  • neurodegenerative diseases
  • osteoarticular disease
  • cancer
  • susceptibility to infection
  • often multiple pathologies are present
  • iatrogenic disease is common
218
Q

Name some common cardiovascular diseases

A
  • hypertension
  • atheroma
    • peripheral vascular disease
    • cerebrovascular disease
    • coronary artery disease
  • advanced glycation end products
    • affect cell matrix & matrix-matrix interactions
    • bind to AGE receptors on endothelial cells
      • increase permeability
      • pro-inflammatory
      • pro-coagulant
      • increased matrix production
219
Q

Describe common neurodegenerative disease

A
  • alzheimer type dementia
  • reduced brain weight
  • frontal and temporal atrophy and compensatory ventricular dilation
  • formation of senile plaques and neurofibrillary tangles
  • acceleration of normal ageing process
  • prominent features of downsyndrome
220
Q

Describe the common osteoarticular diseases

A

osteoperosis- reduced density of bone/bone mass, prone to fracture with minimal stress, limbs (falls) and vertebral bodies

  • genetic
  • lifestyle
  • diet
  • failure of osteoblastic activity

osteoarthritis

  • degeneration of articular surface
  • wear and tear

other conditions- Paget’s disease

221
Q

Describe common neoplastic diseases in the elderly

A
  • 1 in 3 develop cancer
  • lung, breast and colon common primary sites
  • multistep hypothesis
    • clinical
    • pathological
    • molecular
  • accumulation of genetic damage that affects members of key families of genes
222
Q

Describe impaired immunity in the elderly

A
  • immune function declines in the elderly
  • prone to infection
    • viral e.g. influenza
    • vaccination policy
  • may develop secondary infections
    • bronchopneumonia
  • reactivation of latent infection
    • varicella zoster (shingles)
    • Mycobacterium TB
223
Q

What three factors is the process of ageing affected by?

A
  • Genetic factors
  • environmental conditions e.g. diet, social
  • manifestation of age related diseases
    *
224
Q

How does cellular ageing come about?

A

Results from a progressive decline in the prolifertive capactiy and life span of the cell

225
Q

Cell ageing is associated with exposure to __________ influences that lead to accumulation of cellular damage at the organelle level that in turn is associated with or results from damage at the molecular level.

A

exogenous

226
Q

What are 3 important structural and biochemical changes that come with cellular ageing

A
  • morphological abnormalities in mitochondria, reduced ER, distorted golgi apparatus
  • accumulation of lipofuscin, advanced glycation end products and abnormally folded proteins
  • attenuation of capacity to undertake key biochemical processes
    • decreased oxidative phosphorylation
    • synthesis of key nucleic acids and proteins/enzymes is reduced
    • reduced capacity for nutrient uptake
227
Q

________ are key factors which influence ageing. DNA _______ pathways are of paramount importance when it comes to genes and ageing.

A

Genes

repair

228
Q

What is longevity in families due to?

A

mitochondria, maternal inheritance

229
Q

What does accumulation of lipofuscin reflect?

A

Episodes of oxidative damage to the cell.

230
Q

The expression of which proteins are altered in senescence?

A
  • beta-galactosidase
  • increased p53, p21, p16 and other cdk inhibitors
231
Q

Where do senescent cells accumulate over time?

A

In somatic tissues

232
Q

When is cellular senscence particularly important?

A

When stem cell populations are affected

233
Q

How is senscence associated with feautres that characterise ageing?

A

With senescence there is reduced capacity for replacing lost or damaged cells therefore compromising normal tissue homeostasis so it is associated with features that characterise ageing.

234
Q

What is the name given to the fixed number of divisions cells go through?

A

Hayflick number

235
Q

Do cells from children or the elderly go through more rounds of division?

A

Children

236
Q

Some genetic abnormalities are associated with much reduced capacity for rounds of cell division- What is Werner’s syndrome associated with?

A

Defective DNA helicase

237
Q

what are telomeres?

A

DNA caps at chromosome ends

repeat sequences TTAGGG

238
Q

What do telomeres do?

A

ensure complete replication of genome and protect coding sequences at the chromosome ends from “damage”

239
Q

What happens to telomeres after each round of cell division

A

There is slight shortening of telomeres

240
Q

What is the function of telomerase?

A

Maintains telomere length.

241
Q

What is telomorase composed of?

A

RNA protein complex- RNA a template for telomere maintenance.

242
Q

Is telomerase present in somatic cells?

A

No only germ and stem cells, so somatic cells undergo replicative senescence

243
Q

Is temolerase expressed in immortalised cells?

A

Yes

244
Q

How does replicative senescence come about?

A
  • telomere shortening
  • other mechanisms of activation of senescence eg hyperproliferation stimulated by activated oncogenes
  • 2 key pathways: p53-p21 and p16INK4A-Rb
245
Q

Describe telomere shortening and the outcomes

A
  • incomplete replication of chromosome ends
  • sensed as a double strand break
  • triggers DNA damage response
  • ATM kinase activates p53 response leading to cell cycle arrest and onset of senescence
  • potentially also protective againsst development of cancer
246
Q

Why do animal models with shortened telomeres show signs of ageing and how is their phenotype rescued?

A
  • loss of stem cell resevoir through apoptosis and senescence
  • phenotype rescued by inactivation of p53 pathways
247
Q

Does p53 inhibit or promote senescence?

A

p53 can inhibit or promote senescence by either increasing or reducing ROS.

248
Q

What is the role of p53 in senescence?

A

p53 regulates transcription of genes encoding anti-oxidant enzymes such as SOD.

  • reduce active ROS and repress senscence (and onset of ageing)
249
Q

DNA damage activating p53 can cause a spike in production of ROS, what does this promote?

A

Senescence and cell death

250
Q

What does physiological p53 protect against?

A
  • Cancer development
  • senescence
  • ageing
251
Q

What does excessive p53 activity lead to?

A

protects against cancer but promotes senescence and ageing

252
Q

Describe progeria

A
  • rare genetic condition
  • usually spontaneous mutation
  • children have normal mental development for actual age
  • in infancy develop growth retardation with macrocephaly and develop signs of old age
  • usually die as a result of atherosclerosis and its consequences
  • life expectancy: late teens to 30 years
253
Q

Ageing at the tissue and cellular level has a scientific basis. What are the genetic and environmental factors?

A

Genetic Factors

  • DNA repair defects
  • orher genetic abnormalities eg IGF-1 pathway

Environmental factors

  • environmental insults/toxins
  • reduced proteosomal activity
254
Q

What are 3 inhibitors of apoptosis?

A
  • growth factors
  • cell matrix components
  • viral proteins
255
Q

What are the inducers of apoptosis?

A
  • withdrawal of growth factors
  • loss of matrix attachment
  • viruses
  • free radicals
  • ionising radiation
  • DNA damage
  • Fas ligand/CD95 interaction
256
Q

What are the molecular mediators and regulators of apoptosis?

A

Extrinsic pathway- death receptors eg CD95/Fas ligand

Intrinsic pathway

  • increased mitochondrial permeability
  • Bcl-2 family
  • cytochrome c/Apaf 1
  • can induce OR inhibit

Caspases-cascade

p53

257
Q

What can lead to increased apoptosis?

A

AIDS

neurodegenerative disorders

reperfusion injury

258
Q

What can lead to decreased apoptosis?

A

Neoplasia

Auto-immune disease

259
Q

Do benign lesions spread in the body/metastasise?

A

NO

260
Q

What is tissue homeostasis a compromise between?

A

Cell division and cell loss

261
Q

What factors lie between extreme cell division and cell loss at a point of homeostasis?

A

Cell size, cell function, tissue organisation, regulation of induction of senescence.

262
Q

Define hyperplasia

A

An increase in cell number in response to a stimulus which regresses on withdrawal of the stimulus.

263
Q

What is the result of hyperplasia?

A

Increased size/volume of an organ or tissue

264
Q

Is hyperplasia pathological or physiological?

A

It may be both, can be compensatory/regenerative.

265
Q

Which hormonally sensitive organs are subject to hyperplasia?

A
  • endometrium
  • breast
  • thyroid
266
Q

Define neoplasia

A

A neoplasm is an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissues, and persists in the same excessive manner after cessation of the stimuli that evoked the change.

267
Q

What are the 2 classifications of neoplasms?

A

Benign or malignant

  • malignant neoplasms= cancer
  • many different forms of benign and malignant tumours
  • detailed classification based on histological features.
268
Q

Describe benign neoplasms

A
  • usually present as a localised mass lesion
    • incidental finding
    • local symptoms
    • functional symptoms (endocrine lesions)
  • usually well circumscribed
  • resemble normal tissue- well differentiated
  • expansile growth- no invasion- circumscribed
  • may be encapsulated
  • no necrosis
  • minimal pleomorphism
  • N:C ratio normal
  • few mitotic figures
  • mitotic figures are normal
  • nuclei not hyperchromatic
  • diploid
  • NO DESTRUCTIVE INVASION
  • DO NOT METASTASISE
269
Q

How are benign neoplasms cured?

A

By surgical incision. At some sites can be difficult to remove- significant clinical implications.

270
Q

How do you classify a benign neoplasm in squamous epithelium?

A

Squamous papilloma

271
Q

How do you classify a benign neoplasm in glandular epithelial tissue?

A

Adenoma

272
Q

What is the name given to a benign neoplasm in fat?

A

Lipoma

273
Q

What is the name given to benign neoplasms found in endothelium?

A

Angioma

274
Q

What is the name given to a benign neoplasm in chondrocytes?

A

chondroma

275
Q

What is the name given to a benign neoplasm in osteoblasts?

A

osteoma

276
Q

What is the name given to a benign neoplasm in smooth muscle?

A

leiomyoma

277
Q

What is the name given to a benign neoplasm in skeletal muscle?

A

Rhabdomyoma

278
Q

Describe malignant neoplasms

A
  • invasive growth pattern- with rapid growth may still look circumscribed
  • not encapsulated
  • can resemble normal tissue but degree of differentiation is variable
  • necrosis common
  • N:C ratio- increased
  • pleomorphic
  • mitotic figures more frequent
  • abnormal mitotic figures
  • nuclei hyperchromatic
  • aneuploid (abnormal no. of chromosomes)
  • LOCALLY INVASIVE AND MAY METASTISISE
279
Q

What is the name given to a malignant neoplasm found in squamous epithelial tissue?

A

Squamous carcinoma

280
Q

What is the name given to malignant neoplasms in glandular epithelial tissue?

A

Adenocarcinoma

281
Q

What is the name given to malignant neoplasms found in fat cells?

A

liposarcoma

282
Q

What is the name given to malignant neoplasms found on chondrocytes?

A

Chondrosarcoma

283
Q

What is the name given to malignant neoplasms found in osteoblasts?

A

Osteosarcoma

284
Q

What is the name given to malignant neoplasms found in smooth muscle?

A

leiomyosarcoma

285
Q

What is the name given to malignant neoplasms found in skeletal muscle?

A

Rhabdomyosarcoma

286
Q

Name some types of malignant tumours?

A
  • glioma Save
  • lyphoma
  • melanoma
  • seminoma
  • mesothelioma
  • eponymous names e.g. Hodgkin’s disease, Ewing’s sarcoma
287
Q

What is a teratoma?

A

A type of germ cell tumour that may contain several different types of tissue such as hair,

288
Q

What is a hamartoma?

A

Mostly a benign mass of disorganized tissue native to a particular anatomical location.

289
Q

How do carcinomas tend to metastasise versus sarcomas?

A

Carcinomas tend to metastasise to regional lymph nodes.

Sarcomas tend to metastasise by the blood stream.

290
Q

Why is it important to classify cancer types?

A

Different cancer types:

  • behave in different ways
  • respond to different forms of treatment
  • have different prognostic outlooks.
291
Q

Name some common forms of cancer

A
  • breast
  • lung
  • colorectal
  • prostate
  • skin- melanoma
  • ovarian/endometrial
  • head & neck cancers
  • gastro-oesophageal
  • lymphoma/leukaemia
292
Q

What are the 3 properties of cancer?

A
  • A mass lesion- disorder of growth
  • locally destructive- invasive
  • capacity to metastasise
293
Q

What are the 6 hallmarks of cancer?

A
  1. self sufficiency in growth signals
  2. insensitivity to anti-growth signals
  3. limitless replicative potential
  4. evade apoptosis
  5. sustained angiogenesis
  6. tissue invasion and metastasis
294
Q

What are the 4 key elements in cancer development?

A
  • genomic instability- defective DNA repair mchanisms
  • Epigenetic changes- reversible, heritable altered gene expression without mutation.
  • stromal micro-environments
  • metabolic alterations
295
Q

Name the components of a neoplasm/neoplastic cell

A
  • blood vessels
  • inflammatory cells
    • macrophages
    • lymphocytes
    • polymorphs
  • fibroblasts
  • stroma
296
Q
A

Principles (10 decks)

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